Basics

Description

A chronic liver disease causing hepatocellular injury and inflammation due to accumulation of fat

Nonalcoholic steatohepatitis (NASH) is part of the spectrum of nonalcoholic fatty liver disease (NAFLD), which is defined as hepatic steatosis (on imaging or histology) without secondary causes for fat accumulation (excessive alcohol consumption, use of medications that may induce steatosis, or hereditary disorders).

Unlike NAFLD with simple steatosis, NASH is potentially progressive and may result in cirrhosis, liver failure, and (rarely) hepatocellular cancer.

Epidemiology

Since NASH was first identified in 1980, it has been increasingly recognized.

NAFLD is the most common liver disease in the United States.

NAFLD prevalence in the United States is 10–35%.

The prevalence of NASH in the general population ranges between 1.5% and 6.45% (1).

The prevalence of NAFLD increases with age.

Age-adjusted prevalence of NAFLD is highest in Mexican Americans, followed by non-Hispanic whites, and is lowest in non-Hispanic blacks.

There is little data regarding the incidence of NAFLD in the general population.

Etiology and Pathophysiology

The pathogenetic processes of NAFLD and its progression are multifactorial—influenced by environmental and genetic factors.

NAFLD is the hepatic manifestation of metabolic syndrome.

Insulin resistance leads to decreased inhibition of lipolysis and increased de novo lipogenesis. Free fatty acids are inappropriately shifted to nonadipose tissues, including the liver.

Apoptosis and oxidative stress contribute to the development and progression of NASH.

Hepatic mitochondrial dysfunction is central to the pathogenesis of NAFLD.

Two-hit hypothesis: Although NAFLD and NASH can remain stable for years, a second hepatic insult (e.g., cytokine-mediated inflammation, lipid peroxidation, or apoptosis) may trigger progression to cirrhosis.

Risk Factors

NAFLD occurs in individuals with components of metabolic syndrome, which increases the risk of NAFLD 4- to 11-fold.